It has been recently found that empagliflozin improves β cell function independently of the "deregulation of glucotoxicity" 2022EASD

Translator: Liao Zhanlin The First Hospital of Nanping City, Fujian Province

Introduction: From September 19 to 23, 2022, the international conference in the field of endocrinology "2022 European Association for Diabetes Research Annual Meeting" was held
in Stockholm, Sweden in the form of "online + offline".

At the meeting, some scholars shared a research report
entitled "Empagliflozin improves the β cell function of patients with type 2 diabetes mellitus without relying on sugar toxicity relief".

Exploration of mechanisms by which empagliflozin improves β cell function

SGLT2 inhibitors are currently thought to improve β cell glucose sensitivity and insulin sensitivity in patients with type 2 diabetes
.

This effect has previously been attributed to glycosis relief, but few studies have explored changes after controlling for differences in
blood glucose.

Therefore, we first explored the role of empagliflozin in the change of glucose sensitivity in β cells, and then explored peripheral insulin sensitivity (IS) and compared
it with insulin therapy when blood glucose control levels are similar.

The study was designed in a two-stage randomized crossover trial with an average age of 58±3 years, an average BMI of 329±0.
9 kg/m2, an average baseline HbA1c of 52.
4± 2.
4 mmol/L, and an average duration of 8.
9 ± 1.
3 years, with a male-to-female ratio of 13:14
.

Participants were randomly given 5 weeks of empagliflozin therapy (group E) and NPH insulin (group I) in each phase, with a 3-week treatment interval between the two stages
.

Requiring I treatment for blood glucose control is similar to E therapy; An OGTT trial
with stable tracking of intravenous and oral glucose was performed before and after each stage of treatment.

β cell function improvement is not an increase in glucotoxicity or an increase in intestinal pancreatic secretion

➤Compared with baseline, both E treatment group and I treatment group had lower blood glucose and similar blood glucose reduction levels (fasting blood glucose -1.

➤ E group Fasting insulin concentration lower 92±12 vs 180±27 pmol/L) (p<0.

➤ The fasting glucagon concentrations were similar in the two treatment groups (19±1 pmol/L vs 19.

➤ Group E had higher prehepatic insulin release (ISR) in response to OGTT (AUC1814±170pmol/kg vs 1599±144pmol/kg) (p=0.

➤ There was no significant difference in postprandial blood glucose fluctuations treated in 2 groups;

➤It can be confirmed that β cells in group E are more sensitive to glucose (0.

➤Fasting liver glucose production increased in group E compared with group I (19.

Group E IS (AUC glucose Rd, tissue/AUC insulin) was significantly lower; However, group I had a decrease compared with the treatment interval (0.

➤ Group E adipose tissue insulin resistance (Adipo-IR: fasting free fat x fasting insulin) is lower [77±11 vs 110±17 mmol/Lxpmol/L, (p=0.
01)];

➤ Group E had higher glucagon AUC (5286±255 vs 4818±345 pmol/min/L) (p=0.
04).

conclusion

During empagliflozin therapy β cell function is not due to relief of glucotoxicity or increased intestinal insulin secretion, peripheral hyperinsulinemia induces insulin resistance
.

Introduction of translators

Liao Zhanlin

Master of Medicine

He currently presides over a project of Fujian Provincial Science and Natural Foundation

Good at diabetes, thyroid disease, adrenal disease diagnosis and treatment
.